Regulation of ligands for the NKG2D activating receptor

By D. Raulet, S. Gasser, Benjamin G. Gowen, W. Deng, Heiyoun Jung. Annual Review of Immunology, 2013

815 citations recorded by the source corpus.

NKG2D is an activating receptor expressed by all NK cells and subsets of T cells. It serves as a major recognition receptor for detection and elimination of transformed and infected cells and participates in the genesis of several inflammatory diseases. The ligands for NKG2D are self-proteins that are induced by pathways that are active in certain pathophysiological states. NKG2D ligands are regulated transcriptionally, at the level of mRNA and protein stability, and by cleavage from the cell surface. In some cases, ligand induction can be attributed to pathways that are activated specifically in cancer cells or infected cells. We review the numerous pathways that have been implicated in the regulation of NKG2D ligands, discuss the pathologic states in which those pathways are likely to act, and attempt to synthesize the findings into general schemes of NKG2D ligand regulation in NK cell responses to cancer and infection.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/5d2b316aa108fa568eab8e6aafd964d4ed673ab2

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Citations in the corpus

The Immunological Synapse (2014, background): “potentially important in recognition of deranged host cells (69, 76).”
Roles of the immune system in cancer: from tumor initiation to metastatic progression (2018, background): “Indeed, in mice, aberrant cell proliferation induces production of the ligand retinoic acid early transcript 1 (RAE1), which is recognized by the stimulatory receptor NKG2D, expressed on NK cells (Raulet et al. 2013).”
The head and neck cancer immune landscape and its immunotherapeutic implications. (2016, background): “This is mediated largely by their NKG family of receptors and their respective ligands, which are preferentially expressed on infected cells and tumor cells (68, 69).”
Mechanism of action of conventional and targeted anticancer therapies: reinstating immunosurveillance. (2013, background): “…agents (Soriani et al., 2009), histone deacetylase inhibitors (Berghuis et al., 2012), and lenalidomide (Benson et al., 2011) reportedly increase the susceptibility of cancer cells to lysis by specific lymphocyte populations (mostly NK, NKT, and gd T cells) (Chan et al., 2010; Raulet et al., 2013).”